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星形细胞上调基因-1(AEG-1)可被脂多糖诱导,作为 toll 样受体 4(TLR4)配体,调节 TLR4 信号通路。

Astrocyte elevated gene-1 (AEG-1) is induced by lipopolysaccharide as toll-like receptor 4 (TLR4) ligand and regulates TLR4 signalling.

机构信息

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.

出版信息

Immunology. 2009 Sep;128(1 Suppl):e700-6. doi: 10.1111/j.1365-2567.2009.03063.x. Epub 2009 Feb 9.

DOI:10.1111/j.1365-2567.2009.03063.x
PMID:19740331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2753960/
Abstract

Astrocyte elevated gene-1 (AEG-1) is induced by human immunodeficiency virus 1 (HIV-1) infection and involved in tumour progression, migration and invasion as a nuclear factor-kappaB (NF-kappaB) -dependent gene. The involvement of AEG-1 on lipopolysaccharide (LPS) -induced proinflammatory cytokine production was examined. AEG-1 was induced via NF-kappaB activation in LPS-stimulated U937 human promonocytic cells. AEG-1 induced by LPS subsequently regulated NF-kappaB activation. The prevention of AEG-1 expression inhibited LPS-induced tumour necrosis factor-alpha and prostaglandin E(2) production. The AEG-1 activation was not induced by toll-like receptor ligands other than LPS. Therefore, AEG-1 was suggested to be a LPS-responsive gene and involved in LPS-induced inflammatory response.

摘要

星形细胞上调基因-1(AEG-1)可被人类免疫缺陷病毒 1(HIV-1)感染诱导,并作为核因子-κB(NF-κB)依赖性基因参与肿瘤的进展、迁移和侵袭。本研究旨在探讨 AEG-1 是否参与脂多糖(LPS)诱导的促炎细胞因子产生。LPS 刺激 U937 人单核细胞前体细胞后通过 NF-κB 激活诱导 AEG-1。LPS 诱导的 AEG-1 随后调节 NF-κB 激活。抑制 AEG-1 表达可抑制 LPS 诱导的肿瘤坏死因子-α和前列腺素 E2 的产生。除 LPS 以外的 Toll 样受体配体不能诱导 AEG-1 的激活。因此,AEG-1 可能是 LPS 反应性基因,并参与 LPS 诱导的炎症反应。

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Clin Cancer Res. 2008 Jun 1;14(11):3319-26. doi: 10.1158/1078-0432.CCR-07-4054.
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Hsp72 induces inflammation and regulates cytokine production in airway epithelium through a TLR4- and NF-kappaB-dependent mechanism.热休克蛋白72(Hsp72)通过Toll样受体4(TLR4)和核因子κB(NF-κB)依赖性机制诱导气道上皮炎症并调节细胞因子产生。
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